An experimental study of surface injury to articular cartilage and enzyme responses within the joint.

An experimental model of degenerative joint disease on chondromalacia consists of a surgically-scarified articular surface of the adult dog knee joint. In 52 dogs, evaluated by histologic and enzymatic assays over a period of 1 to 110 weeks post-surgery, the levels of acid hydrolase activity varied on various areas of articular cartilage within the same joint. There was a transient rise in most of the acid hydrolases in the synovium as a response to arthrotomy of the knee joint. All of the acid hydrolases studied did not respond uniformly to surgically created trauma. There was evidence of repair of the cartilage lacerations even when the subchondral zone was not breached. Lacerations in the central portion of the patella rarely showed healing in contrast to those placed more to the periphery of the articular surface. There was no gross or histologic evidence of progressive degenerative joint disease up to 2 years post-surgery. Thus an injury inflicted to the surface of the articular cartilage may be in itself insufficient in severity to produce destructive changes in the joint. This should not be too surprising, since, clinically, all joint surface injury does not lead to degenerative arthritis. The joint seems to have an injury threshold whereby chondrocytes are capable of repairing surface injury if the damage is not massive or repetitive. Insofar as lacerations in the center of the patella rarely healed, while the peripheral ones showed consistent signs of healing, the site of injury, as well as the magnitude of injury, may be critical.